Transforming growth factor beta signaling is recognized for its essential role in embryogenesis in deuterostomes and arthropod protostomes. The tropical disease Schistoromiasis is caused by the metazoan parasite Schistosomes, classified by the lophotrochozoan phylum Platyhelminthes. Activation of the TGF-beta signaling in metazoans begins at the cell surface when a dimeric ligand binds to a complex composed of types 1 and 2 serine/theorine kinase receptors. Due to ligand binding, type 2 serine/theorine kinase receptors phosphorylates (gives a phosphate group from a high energy molecule such as ATP) type 1 serine/theorine kinase receptor site, activating it, and causes it to phosphorylate cytoplasmic Smad protein, which translocates to the nucleus and mediates gene expression. Components of a functional TGF-β pathway(s) includes one type I receptor, Schistosoma mansoni receptor kinase-1 known as SmRK1, Schistosoma. mansoni transforming growth factor-β type I receptor known as SmTβ RI, one type II receptor known as SmRK2 and SmTβ RII, and three Smads, have been identified in Schistosoma. mansoni, with components localized to either the surface of the fluke or reproductive tissues of the female fluke.
The male and female Schistosomes enter the human blood vessels by cutting its way through the outside layer of the human skin, where the flukes feed on hemoglobin. Sexual production later occurs within the mesenteric vasculature, where the female fluke produces approximately 300 eggs per day. Development of an immature egg to a mature egg that contains a miracidum takes approximately 5 days. The egg travels from the veins into the small intestines, and through the digestive path with the intestines to be released within the feces into the external environment. Many of the eggs do not reach external environment as they become trapped within the host tissues causing an immune response to the egg antigens, and some are swept into the liver where they cause granulomas on the liver, obstructing the portal veins and causing enlargement of the liver.
TGF-beta homologue SmInAct is necessary for the formation of Schistosomiasis monsani as shown in RNA interference studies indicating that infertile Schistosomes have a deficit of SmInAct protein. The formation of SmInAct is controlled by TGF-beta signalling, where the initiation of the mediation of the gene is caused by the release of TGR beta protein from the male Schistosome onto the serine/theorine receptor site 2 on the female Schistosome. 
An inhibitor or antagonist represses and prevents another molecule from engaging in a reaction through blocking the pathway necessary for the reaction, such as physically blocking the pathway necessary for a molecule to reach a receptor site. Trk receptor sites are serine/theorine kinase receptors found on female Schistosomes necessary for the TGF-beta signaling caused by TGR beta protein for the formation of SmInAct. Inhibitor Trk receptor agents act as inhibitors or antagonist that prevent TGR beta protein from reacting to Trk receptor sites. Due to the numerous Inhibitor Trk receptor agents, solely the Trk inhibitor Decorin will be focused on within the introduction. Decorin is coded by the DCN gene found within the human genome. (Decorin, a ubiquitous small cellular or pericellular matrix proteoglycan, belongs to the small leucine-rich proteoglycan (SLRP) family and consists of a core protein and a covalently linked glycosaminoglycan chain of either chondroitin sulfate or dermatan sulfate. Decorin is a component of connective tissue that interacts with several extracellular matrix components, such as type I collagen and fibronectin, and plays a role in matrix assembly. Decorin core protein also binds to growth factors such as TGF-beta, and the decorin endocytosis receptor. Decorin can suppress the growth and the metastasis of a wide range of cancer cells in vitro by attenuation of the EGFR-mediated intacellular signaling and induction of apoptosis. Decorin can be found within the human urine, where surplus production of Decorin is released within the human urine, assuring the safety of the use of Trk receptor site Decorin as the body naturally releases the overproduction of decorin through the urinary system.
Several Inhibitor Trk receptor agents correspond to DNA sequences within the genome of living organisms for natural production of the inhibitor. The corresponding DNA sequence can be obtained through placing the cell of an organism within a solution containing lysosomes and SDS buffers, then centrifuging the solution within the corresponding machine and precipitating the DNA with cold ethanol. The corresponding DNA sequence can then be located using several methods, including but not restricted to Southern blotting with radioisotope probes that anneal to the nucleic acids of the corresponding DNA sequence. The DNA sequence can then be removed by digesting the DNA with the corresponding restriction enzymes. Once the DNA sequence possessing the gene for production of Inhibitor Trk receptor agents is obtained, it can be placed in several organisms such as rice plants or probiotic bacteria. The biolostic method can be used to insert DNA within the genome of rice plants, resulting in Inhibitor Trk receptor agents within the rice grown from the plant. Probiotic bacterial lives within the human body in mutualism due to the bacteria's beneficial effect to humans. Bacteria holds ring shaped plasmids with the ability of carrying genetic information in and out of the bacteria. Using the restriction enzymes used to cleave DNA sequence, one can cleave the plasmid and insert the Inhibitor Trk receptor agent gene within the plasmid with DNA ligase. Several methods can then be used to insert the plasmid into its corresponding pro-bacteria (or probacteria), genetically modifying the probacteria into allowing the bacteria to produce Inhibitor Trk receptor agents. Selecting probiotic bacteria that lives near the mesontatic veins will allow the formation of Inhibitor Trk receptor agents, inhibiting female Schistosomes from producing eggs.